INTRODUCTION β-Asarone is a major component of Acorus tatarinowii Schott. It has pharmacological effects that include antihyperlipidemic, anti-inflammatory, and antioxidant activity. In the present study, the effect of β-asarone on neurodegeneration induced by intrahippocampal administration of β-amyloid was investigated in adult male Wistar rats. MATERIAL AND METHODS The rats were randomly divided into 9 groups: normal control, sham-operated control, β-asarone (12.5, 25, and 50 mg/kg intragastrically, daily) alone, Alzheimeric control rats (β-amyloid, intrahippocampal), β-asarone (12.5, 25, and 50 mg/kg intragastrically, daily) together with β-amyloid, and treatment was performed accordingly. Animals were injected with β-amyloid bilaterally. Animals received β-asarone daily using an intragastric tube for 50 days, starting from 30 days before administration of the β-amyloid. The rats were sacrificed and parameters of oxidative stress, superoxide dismutase (SOD) and glutathione peroxidase (GPX) activity were measured in hippocampus homogenate. Histopathological changes were examined by Bielschowsky staining. RESULTS Our results showed that administration of β-asarone (25 and 50 mg/kg) significantly increased the levels of antioxidant enzymes, including SOD (1.09 ±0.02, 1.21 ±0.02, p < 0.001, respectively) and GPX (58.94 ±0.78, 68.92 ±3.64, p < 0.001, respectively) in comparison with Alzheimeric control rats (SOD and GPX level for Alzheimeric control group: 0.44 ±0.01, 35.09 ±1.15, respectively). Histopathological examination showed that β-asarone decreased cell loss in the cerebral cortex and hippocampus in Alzheimeric rats. CONCLUSIONS These results indicate that β-asarone is effective in providing protection against oxidative stress and neuronal damage induced by β-amyloid.

中文翻译：

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β-细辛醚对正常和 β-淀粉样蛋白诱导的阿尔茨海默病大鼠的影响。

引言 β-细辛醚是 Acorus tatarinowii Schott 的主要成分。它具有药理作用，包括抗高血脂、抗炎和抗氧化活性。在本研究中，在成年雄性 Wistar 大鼠中研究了 β-细辛醚对海马内注射 β-淀粉样蛋白诱导的神经变性的影响。材料与方法 将大鼠随机分为9组：正常对照组、假手术组、单独β-细辛（12.5、25、50 mg/kg灌胃，每日），阿尔茨海默病对照组（β-淀粉样蛋白，海马内）， β-细辛醚（12.5、25 和 50 mg/kg 灌胃，每日）与 β-淀粉样蛋白一起进行相应的治疗。动物双侧注射β-淀粉样蛋白。动物每天使用胃内管接受 β-细辛醚 50 天，从给予β-淀粉样蛋白前30天开始。处死大鼠并在海马匀浆中测量氧化应激、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GPX）活性的参数。通过 Bielschowsky 染色检查组织病理学变化。结果 我们的结果表明，给予 β-细辛醚（25 和 50 mg/kg）显着增加抗氧化酶水平，包括 SOD（分别为 1.09 ±0.02、1.21 ±0.02、p < 0.001）和 GPX（58.94 ±0.78， 68.92 ±3.64，p < 0.001，分别）与阿尔茨海默病对照组大鼠比较（阿尔茨海默病对照组的 SOD 和 GPX 水平：分别为 0.44 ±0.01、35.09 ±1.15）。组织病理学检查表明，β-细辛可以减少阿尔茨海默病大鼠大脑皮层和海马的细胞损失。